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Ciccarone Center Research

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Cholesterol / Lipids / Statins

Landmark Articles

What role does genetics play in the variability in response to statin therapy?
By: Patel J, Abd T, Blumenthal RS, Nasir K, Superko R.
We examine the role of certain genetic polymorphisms in affecting the response to statin therapy.
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Discordance in lipid measurements: Can we capitalize to better personalize cardiovascular risk assessment and treatment?
By: Cruz D, Ahmed H, Jones S, Elshazly M, Martin S.

Lipid measurement is one of the cornerstones of cardiovascular risk assessment and treatment. It is widely accepted that reduction of atherogenic lipids reduces risk of atherosclerotic cardiovascular disease. As the study of lipids has yielded deeper understanding of the pathophysiology of lipid metabolism, it has become clear that different techniques to quantify atherogenic lipids and lipoproteins could be complementary. For example, low-density lipoprotein cholesterol can exist in a range of forms from small, dense to large, buoyant, and therefore, discordance may arise between measures of its cholesterol content and particle concentration. In this article, we review the most recent literature on discordance in lipid measurements. We emphasize interesting and important new findings, and aim to bring the reader up-to-date on the topic. We submit that lipid discordances create an opportunity to better personalize the risk assessed for atherogenic cardiovascular disease and the care we give patients with dyslipidemia. We note that while prior research has often examined one lipid measure vs another in their abilities to predict the average risk in a population, recent studies are increasingly asking what lipid discordance in individual patients can tell us about risk. We propose that this latter approach asks the more clinically important question. The message from these studies is consistent: discordance matters. As the field moves forward, we propose standardization of methods for discordance research. In our view, this will best enable us to further clarify the clinical implications of the principle of discordance and best inform personalized cardiovascular care.

How do statins work?: Changing paradigms with implications for statin allocation.
By: Blaha MJ, Martin SS.
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Derivation and validation of a novel method for more accurate estimation of LDL-C from the standard lipid profile.
By: Jones SR, Martin SS.

Low-density lipoprotein cholesterol (LDL-C) is of longstanding clinical and research interest and the primary target in national and international clinical practice guidelines. Conventionally, LDL-C is estimated by the Friedewald equation which assumes a fixed ratio of TG:VLDL-C of 5:1. Applying a factor of 5 to every individual patient is problematic given variance in the TG:VLDL-C ratio across the range of triglyceride and nonHDL-C levels. Rather than a fixed conversion factor, we have developed a method that uses a sliding scale factor to estimate VLDL-C with high precision from triglycerides and non-HDL cholesterol levels.

Effect of statin treatment on coronary plaque progression — a serial coronary CT angiography study.
By: Zeb I, Li D, Nasir K, Malpeso J, Batool A, Flores F, Dailing C, Karlsberg RP, Budoff M.

Statin therapy resulted in significantly lower progression of low attenuation plaque and noncalcified plaques compared to nonstatin users.

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APOE modulates the correlation between triglycerides, cholesterol, and CHD through pleiotropy, and gene-by-gene interactions.
By: Maxwell TJ, Ballantyne CM, Cheverud JM, Guild CS, Ndumele CE, Boerwinkle E.
The relationship between total cholesterol and triglycerides varies by apolipoprotein E isoform genotype in African-American and European-American populations.
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Comparison of a novel method vs the Friedewald equation for estimating low-density lipoprotein cholesterol levels from the standard lipid profile.
By: Martin SS, Blaha MJ, Elshazly MB, Toth PP, Kwiterovich PO, Blumenthal RS, Jones SR.
This study sought to develop a new method for calculating low-density lipoprotein cholesterol, the so-called “bad” form of blood fat that can lead to hardening of the arteries, that would be more accurate than the standard profile for measuring a person’s risk for heart attack and stroke.
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Non-high-density lipoprotein cholesterol, guideline targets, and population percentiles for secondary prevention in 1.3 million adults: the VLDL-2 study (very large database of lipids).
By: Elshazly MB, Martin SS, Blaha MJ, Joshi PH, Toth PP, McEvoy JW, Al-Hijji MA, Kulkarni KR, Kwiterovich PO, Blumenthal RS, Jones SR.
There is a significant patient-level discordance between non-HDL-C and LDL-C percentiles at lower LDL-C and higher triglyceride levels, which has implications for the treatment of high-risk patients.
Read on Pubmed
Is direct measure of LDL preferred over a calculated LDL?
By: Miller PE, Elshazly MB, Jones SR, Martin SS.
Ratio of dense to buoyant LDL subclass is associated with LDL density phenotype (VLDL-5).
By: Ahmed HM, Elshazly MB, Blaha MJ, Martin SS, Kulkarni K, Jones SR.

Dense LDL phenotypes are associated with increased atherogenicity, and are commonly evaluated for the purposes of atherosclerosis research and cardiovascular risk discrimination. In this study we examined the ability of LDL subclasses, expressed as a ratio of dense-to-buoyant subclass (LLDR), to predict LDL density phenotype. Further research is needed to investigate the relationship between lipoprotein density and size, and whether LLDR provides more cardiovascular risk discrimination than LDL density phenotype.